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Year 2 BB > YR2 BB OVERVIEW > Flashcards

YR2 BB OVERVIEW Flashcards

1
Q

Ganglion vs nucleus

A

Ganglion - PNS - one exception is the basal ganglia

Nucleus - CNS

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2
Q

Function of the basal ganglia

A

Regulate the intensity of movements
Inhibit antagonistic/unnecessary movements
Regulate attention and cognition
Motor program switch - from resting state

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3
Q

(Dorsal) striatum

A

Caudate + putamen

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4
Q

Corpus striatum

A

Striatum (c+p) + globus pallidus

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5
Q

Lentiform nucleus

A

Putamen + globus pallidus

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6
Q

Location of substantia nigra

A

At the base of the midbrain

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7
Q

Ventral striatum

A

Nucleus accumbens

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8
Q

Neurotransmitter input from cortex to dorsal striatum

A

Glutaminergic

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9
Q

Neurotransmitter input from substantia nigra to dorsal striatum

A

Dopaminergic

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10
Q

GABA excitatory or inhibitory?

A

Main inhibitory neurotransmitter of the CNS

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11
Q

D1 receptors excitatory or inhibitory?

A

Excitatory

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12
Q

D2 receptors excitatory or inhibitory?

A

Inhibitory

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13
Q

Summarise the direct pathway of the basal ganglia

A

a

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14
Q

What is the general action of the GPi on the motor thalamus?

A

Tonic inhibition of the motor thalamus to prevent sudden movement

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15
Q

Which direct or indirect pathway is tonically active?

A

Direct pathway

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16
Q

What is the function of the direct pathway

A

Allow for movement (?)

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17
Q

What is the internal capsule?

A

White matter structure separating the caudate from the putamen and the globus pallidus

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18
Q

Primary motor cortex is broadmann area…?

A

4

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19
Q

Location of primary motor cortex

A

Just anterior to the central sulcus

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20
Q

Distribution of the motor homonculous

A

Feet and legs centrally
Hip, trunk and shoulder
Hands and Fingers
Face

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21
Q

Arteries to the basal ganglia

A

Lenticulostriate arteries

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22
Q

Consequence of damage to premotor cortex or supplementary motor cortex

A

Apraxia

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23
Q

Effect on reflexes and muscle strength from apraxia

A

Normal reflexes and muscle strength

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24
Q

Apraxia

A

Inability to perform complex motor movement

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25
Q

Aphasia

A

Inability to understand or produce speech

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26
Q

Motor aphasia

A

Difficulty putting words together in a sentence - will use very simple or short sentences ( no problem understanding)

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27
Q

Consequence of damage to Broca’s area

A

Motor aphasia

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28
Q

Consequence of damage to FEFs

A

Oculomotor aphasia - difficulty moving the eyes horizontally and in following objects

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29
Q

Location of the somatosensory cortex

A

Parietal lobe

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30
Q

Location of prefrontal cortex

A

Right at the front of the frontal lobe (area 9)

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31
Q

Function of prefrontal cortex

A

Involved in the planning of movements and in executive functions

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32
Q

Consequence of damage to prefrontal cortex

A

Personality changes

Lack of ability to plan tasks

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33
Q

Location of orbitofrontal cortex

A

Most anterioinferior region of the frontal lobe (area 11)

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34
Q

Consequence of damage to the orbitofrontal cortex

A

Pseudopsychppathoc behaviour - impulsive, sexual disinhibition, lack of concern for others

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35
Q

Consequence of damage to the motor thalamus

A

Severe paralysis

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36
Q

Input into the corticobulbarpinal tract

A

a

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37
Q

Output from the corticobulbarspinal tract

A

a

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38
Q

Termination of the corticobulbar tract

A

a

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39
Q

Location of decussation of the corticospinal tract

A

aa

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40
Q

Function of corticobulbar tract

A

a

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41
Q

Pyramidal vs. extrapyramidal tracts

A

a

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42
Q

Which horns of the grey matter do pyramidal and extrapyramidal tracts run through?

A

a

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43
Q

Consequence of damage to the reticulospinal tract

A

a

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44
Q

Define spasticity

A

a

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45
Q

Define clonus

A

a

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46
Q

Define hyperrelexia

A

a

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47
Q

Cause of spasticity

A

a

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48
Q

Cause of clonus

A

a

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49
Q

Cause of hyperreflexia

A

a

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50
Q

What are spasticity, clonus and hyperreflexia signs of?

A

a

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51
Q

Decorticate vs decerebrate posturing - presentation and where is the damage?

A

a

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52
Q

What is the clasp knife reflex and what does this indicate damage to?

A

a

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53
Q

Three sites of DBS for treatment of PD

A

a

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54
Q

‘Folia’

A

a

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55
Q

Lobes of the cerebellum

A

a

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56
Q

Cerebellum - primary fissure

A

a

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57
Q

Function of cerebellar nodes

A

a

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58
Q

Function of spinocerebellar tract

A

a

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59
Q

On what side of the body will damage to the cerebllum show?

A

a

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60
Q

On what side of the body will damage to the cortex show?

A

a

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61
Q

Cerebellar nuclei

A

a

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62
Q

Function of vestibulocerebellum

A

a

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63
Q

Function of the spinocerebellum

A

a

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64
Q

Function of the cerebrocerebellum

A

a

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65
Q

What is the neocerebellum?

A

a

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66
Q

Input to neocerebellum

A

a

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67
Q

Output from neocerebellum

A

a

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68
Q

Floclonodular lobe syndrome (damage) presentation

A

a

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69
Q

Anterior lobe syndrome (damage) presentation

A

a

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70
Q

Posterior lobe syndrome (damage) presentation

A

a

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71
Q

Common cause of floculonodular lobe syndrome

A

a

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72
Q

Common cause of anterior lobe syndrome

A

a

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73
Q

Common cause of posterior lobe syndrome

A

a

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74
Q

Nystagmus/pstosis/constricted pupil of just one eye is a sign of what type of damage?

A

a

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75
Q

Symptoms of cerebellar stroke

A

aa

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76
Q

Define dysphagia

A

a

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77
Q

Define dysarthria

A

a

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78
Q

Define ataxia

A

a

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79
Q

Dorsal/ventral is anterior/posterior?

A

a

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80
Q

Dorsal/ventral spinocerebellum is ipsilateral or contralateral?

A

a

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81
Q

Two typical histological signs of PD

A

a

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82
Q

What are the three hallmarks of PD (signs)

A

a

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83
Q

What type of symptoms can DBS be used to treat?

A

a

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84
Q

NEED TO GO OVER THE DIRECT AND INDIRECT PATHWAYS ADN HOW THESE CHANGE WITH PD - ARUN/MIMI???

A

a

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85
Q

MPTP

A

a

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86
Q

Impact of MAO on dopamine

A

a

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87
Q

L-dopa to dopamine via which enzyme?

A

a

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88
Q

Amantadine to treat PD

A

a

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89
Q

Mutation in Huntington’s disease

A

a

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90
Q

What are the four different stages of pain?

A

a

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91
Q

Two types of nociceptors

A

a

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92
Q

TRPV1 nociceptor responds to?

A

a

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93
Q

TRPM8 nociceptor responds to?

A

a

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94
Q

ASIC3 nociceptor responds to?

A

a

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95
Q

Damage to which nociceptor fibres in diabetic neuropathy?

A

a

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96
Q

Two types of c-fibres

A

Peptidergic - release of peptides

Peptide poor - release of ATP

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97
Q

C-fibres project to which part of the lamina in the spinal cord and are carried in which tract?

A

a

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98
Q

D-delta fibres project to which part of the lamina in the spinal cord and are carried in which tract?

A

a

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99
Q

What is present in lamina II of the spinal cord?

A

a

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100
Q

What occurs in lamina V of the spinal cord?

A

a

101
Q

Which part of the brain mediates the unpleasant sensation of pain?

A

a

102
Q

Role of limbic system in pain?

A

a

103
Q

Where do projection neurones decussate?

A

a

104
Q

Function of the amygdala

A

a

105
Q

Explain peripheral sensitisation

A

a

106
Q

Four signs of inflammation

A

a

107
Q

What is central sensitisation?

A

a

108
Q

Define allodynia

A

a

109
Q

Define hyperalgesia

A

a

110
Q

Three signs of central sensitisation

A

a

111
Q

Define chronic pain

A

a

112
Q

Define maladaptive pain

A

a

113
Q

Two types of maladaptive pain

A

a

114
Q

Define innocuous stimuli

A

a

115
Q

Define endogenous modification

A

a

116
Q

Example of endogenous modification

A

a

117
Q

Gate control theory

A

The idea that non-painful input closes the gate to painful input
This prevents pain sensation from travelling to the CNS and so suppresses the level of pain that is felt

118
Q

Neurotransmitters involved in central sensitisation

A

a

119
Q

What are the three cortical components of the limbic system?

A

Cingulate cortex - anterior and posterior
Orbito-frontal cortex
Parahippocampal cortex/gyrus (medial temporal lobe)

120
Q

Infarct to which arteries can result in damage to the limbic system?

A

Anterior cerebral artery

Posterior cerebral artery

121
Q

Define caudal

A

Of or like a tail

122
Q

Function of rostral anterior cingulate cortex

A

Registers that pain has occurred

+potentially what to do in response to this pain

123
Q

Function of caudal anterior cingulate cortex

A

Registers the quality of the pain i.e. how bad on a scale from 1-10

124
Q

Cingulotomy and function

A

Cut into the anterior cingulate cortex to prevent the rostro-caudal flow of fibres
Thought to reduce the emotional distress of pain

125
Q

Function of posterior cingulate cortex

A

Unknown but thought to be involved in visuo-spatial memory

126
Q

Function of parahippocampal cortex/gyrus

A

Involved in learning and memory

127
Q

Function of orbitofronal cortex

A

How to behave in response to anticipated threat - how to avoid pain/injury

128
Q

Overactivity of the orbitofrontal cortex is present in which neurological condition?

A

a

129
Q

Subcortical components of the limbic system

A

a

130
Q

Function of hippocampus

A

Time of day that memory occurred and location that the memory occurred AND the commitment of new memories to the long term memory

131
Q

Anterograde amnesia and cause

A

Failure to transfer new experiences to long term memory

Damage to the hippocampus

132
Q

Function of the amygdala

A

Stimulates feelings of fear and anxiety

Can also stimulate fight or flight response of the sympathetic NS

133
Q

Werknicke-Korsakoffe syndrome and cause

A

a

134
Q

Temporal lobe epilepsy and cause

A

a

135
Q

Septum pallucidum

A

Thin vertical membrane - separates the anterior horns of the left and right lateral ventricles
Runs from corpus callosum to fornix

136
Q

Septum pallucidum

A

Thin vertical membrane - separates the anterior horns of the left and right lateral ventricles
Runs from corpus callosum to fornix

137
Q

Retrograde amnesia and cause

A

No access to the memories prior to an event - damage to the cingulate gyrus

138
Q

Lenticulostriate arteries and origin

A

a

139
Q

Lenticulostriate arteries and origin

A

Blood supply to basal ganglia and the internal capsule

Branches from the MCA

140
Q

Vertebral arteries pass through which foramen?

A

Foramen magnum - then join to form basilar artery

141
Q

Blood supply to the pons

A

Pontine arteries - branches from the Basilar

142
Q

Blood supply to the brainstem

A

PICA - from the vertebral artery

143
Q

Structures piercing the dura

A

Cerebral veins - bridging veins

Arachnoid granulation - CSF

144
Q

MCA stroke presentation

A

a

145
Q

ACA stroke presentation

A

a

146
Q

PCA stroke presentation

A

a

147
Q

PCA stroke presentation

A

a

148
Q

ACA stroke presentation

A

Contralateral sensorimotor loss below the waist
Urinary incontinence
Personality defects
If the corpus callosum is effected - split brain synrome

149
Q

PCA stroke presentation

A

Damage to the temporal lobe - reading and writing deficits, memory deficits
Contralateral homonymous hemianopia

150
Q

Middle meningeal artery is a branch from which artery?

A

Third branch of the maxillary artery

151
Q

Middle cerebral artery vs. middle meningeal artery

A

MCA - continuation of the internal carotid - anterior cerebral blood supply - medially located - within the brain - lentinculostriate arteries branch from here
MMA - blood supply to the meninges - branches from the maxillary artery - laterally located - runs just under the pterion - trauma here leads to extradural haematoma

152
Q

Middle cerebral artery vs. middle meningeal artery

A

MCA - continuation of the internal carotid - anterior cerebral blood supply - medially located - within the brain - lentinculostriate arteries branch from here
MMA - blood supply to the meninges - branches from the maxillary artery - laterally located - runs just under the pterion - trauma here leads to extradural haematoma

153
Q

Bones forming the pterion

A

Frontal, sphenoid, parietal, temporal

154
Q

Cerebral falx and function

A

Septa (dural fold) between the left and right cerebral hemispheres

155
Q

Cerebellum tentorium and function

A

Septa (dural fold) separating the occipital lobe from the brainstem

156
Q

Tentorial notch and function

A

Hole in the cerebellum tentorium allowing for the passage of the brainstem and blood vessels to the middle cranial fossa

157
Q

Two layers of the dura mater

A

Perisoteal layer - closest to the skull

Meningeal layer - next to the arachnoid layer

158
Q

DO THIS QUIZ FOR DURAL VENOUS SINUSES

http://act.downstate.edu/courseware/haonline/quiz/practice/u5/quiztop5.htm

A

DO THIS QUIZ FOR DURAL VENOUS SINUSES

http://act.downstate.edu/courseware/haonline/quiz/practice/u5/quiztop5.htm

159
Q

All layers of meninges from skull to brain

A 
Skull 
Dura - periosteal layer
Dura - meningeal layer 
Arachnoid granulations coming up from the arachnoid mater to drain into venous sinuses
Arachnoid mater 
Subarachnoid space 
Pia mater
Cerebral cortex of brain
160
Q

Imaging bone - x-ray or MRI and why?

A

X-ray - bone is dense and absorbs high level of x-ray energy

161
Q

Imaging CNS - x-ray or MRI and why?

A

MRI - mostly water - will not absorb x-rays

162
Q

T1 weighted MRI - colour of bone, air, blood, CSF

A

Black

163
Q

T1 weighted MRI - colour of fat and bone marrow

A

White

164
Q

T2 weighted MRI - colour of bone, air, blood, CSF

A

White

165
Q

T2 weighted MRI - colour of fat and bone marrow

A

Black

166
Q

Lateral ventricle in relation to the corpus callosum

A

Immediately inferior

167
Q

Fourth ventricle in relation to the cerebellum

A

Immediately anterior to the cerebellum and posterior to the brainstem/spinal cord

168
Q

Consequence of enlarged brain ventricles

A

a

169
Q

Define diffuse head injury

A

Microscopic damage which cannot be demonstrated by any of the current imaging techniques
BUT unconscious patient

170
Q

Define diffuse head injury

A

Microscopic damage which cannot be demonstrated by any of the current imaging techniques
BUT unconscious patient

171
Q

Depressed fracture

A

Area of skull driven inwards

172
Q

Compound fracture

A

Scalp is torn

173
Q

Closed fracture

A

The skin is not broken

174
Q

Comminutive fracture

A

Fragmentation of bone into 2/3 pieces

175
Q

Three theories for the pathophysiology of depression

A

Monoamine theory - serotonin and noradrenaline dysfunction
Dopamine - reduced levels
Decreased grey matter - at the subgenual cingulate prefrontal cortex

176
Q

Which structure is impaired in depression, causing people to focus more heavily on negative thoughts?

A

Prefrontal cortex

177
Q

Reversible MAO inhibitors are selective for what?

A

These are selective for MAOa

178
Q

‘Antidepressant drug discontinuation syndrome’ + how to avoid this

A

Immediate cessation of antidepressants in some individuals can result in adverse side effects - should have a slowly reduced degree of the medication over time

179
Q

What is bipolar disorder? + main treatment

A

Cycles of depression and mania (hyperactivity)

Lithium

180
Q

How long should patients continue to take antidepressants for following remission?

A

At least six months to avoid relapse

181
Q

When to use vagal nerve stimulation for the treatment of depression

A

Chronic depression

182
Q

Advantage of CBT to treat depression

A

Can augment the pharmacological therapy for depression

183
Q

Target of DBS for depression

A

Broadmann’s area 25/subgenual cingulate cortex

184
Q

Depression can result in reduced white and grey matter in which structure?

A

Hippocampus

185
Q

When should citrulline be used for treatment of depression?

A

SRRI - used in patients with heart arrthythmia’s/history of MI

186
Q

Mechanism of action of tricyclic antidepressants

A

These act to reduce the reuptake of monoamines

187
Q

Mechanism of action of SSRIs

A

Reduce reuptake or serotonin (5-HT) specifically

188
Q

‘Cheese effect’

A

Inhibition of both MAOa and MAOb - should avoid certain foods which cannot be digested - consumption of these foods will result in adverse side effects

189
Q

Which antidepressant drug is safe in overdose?

A

SSRIs

190
Q

Fluoxetine - what is this and who should it be prescribed to?

A

SSRI

Used in patients with depression and diabetes - shown to have positive impact on HbA1c

191
Q

Five key symptoms of depression

A 
Anhedonia 
Feelings of guilt/lack of self-worth 
Weight loss/decrease in appetite 
Fatigue
Lack of concentration

(suicidal ideation)

192
Q

Give four non-pharmacological treatment options for depression

A

DBS
Vagal nerve stimulation
Electroconvulsive therapy
CBT

193
Q

Structure of opioid receptors

A

G-protein coupled receptors

194
Q

Three opioid receptors

A

Mu
Kappa
Delta

195
Q

Location of opioid receptors

A

Throughout the body - widespread distribution results in wide range of effects

196
Q

What are enkephalines?

A

Short morphine-like peptide produced naturally in the body

Involved in the regulation of nociception

197
Q

Functions of morphine at receptor

A

Increased potassium conductance and decreased calcium conductance SO reduced excitability of neurone (hyperpolarised) and reduced release of neurotransmitters from neurone

198
Q

Name four common opioid drugs

A

Morphine
Heroin
Dextromaride
Methadone

199
Q

Opioid naxolone - what should you know?

A

This opioid/opiate (interchangable) has a very short half life - never leave patient alone with this

200
Q

Three drastic side effects of opiodes

A

Respiratory depression
Nausea and vomiting
Hypotension

201
Q

Opioid switch

A

Patients can become tolerant to opioids - should then switch to another type

202
Q

Mechanism of action of paracetamol

A

Reduces the active oxidised form of COX-2

Analgesic and antipyretic

203
Q

Mechanism of action of NSAIDs

A

Reduces COX-1 and COX-2 enzymes

204
Q

Five adverse effects of NSAIDs

A 
Arthritis - RA, OA
Gout
Nausea
GI bleeding 
Muscle spasms
205
Q

Medication types used in the treatment of neuropathic pain

A

Anticonvulsants

Tricyclic antidepressants e.g. amitriptyline

206
Q

Name three anticonvulsants and the channels they work on

A

Sodium valproate - sodium channel
Carbamazepine - sodium channel
Pregabalin - calcium channels

207
Q

Action of tricyclic antidepressants

A

Inhibit the reuptake of monoamines

Block both sodium and calcium channels

208
Q

Trigeminal neuralgia

A

Facial syndrome involving one or more of trigeminal nerve branches
Compression/distortion/stretching

209
Q

Symptoms of trigeminal neuralgia

A

Sudden, sharp, stabbing pain sensation

210
Q

Treatment of trigeminal neuralgia

A

Carbamazepine
Baclofen
Phenytoin
Valproate

211
Q

Mechanism of action of local anaesthetic

A

Block sodium channels

212
Q

Substance P

A

Peptide released by the peptidergic nociceptive c-fibres

Released in response to infection/injury and promotes local inflammation

213
Q

Which AEDs increase their own metabolism and how

A

Phenytoin and carbamazepine

These increase hepatic enzymes

214
Q

Imperative treatment for status epilepticus

A

Intravenous benzodiazepine

215
Q

Epilepsy

A

a

216
Q

Different calcium channels

A

aa

217
Q

Calcium channels most involved in epilepsy - what type of seizure?

A

aa

218
Q

Action of pregabalin and gabapentin on epilepsy and mechanism of action

A

a

219
Q

‘Epileptogenesis’

A

a

220
Q

Stages of a tonic-clonic seizures

A

a

221
Q

Safest AEDs to administer in pregnancy

A

a

222
Q

Patient with epilepsy - how many of them will also have a relative with epilepsy?

A

a

223
Q

Declarative vs. non-declarative memory

What memory form are these?

A

Declarative (explicit) - consciously going back in time to recall information
Non-declarative (implicit) - memory acquired and used unconsciously - skills and behaviours e.g. how to perform a dance
Long term memory

224
Q

Two types of declarative memory and what are these?

A

Episodic - going back in time to remember personal events

Semantic - remembering general facts about the world

225
Q

‘Spatial memory’ and region of brain involved in this

A

Memory related to where you are in space
Based on one’s environment and spatial orientation
(Taxi drivers - well developed)

226
Q

Three types of amnesia and what are these?

A

Anterograde - cannot transform new events into long term memory
Retrograde - cannot remember events occurring prior to the onset of amnesia
Dissociative - cannot remember critical personal information about oneself

227
Q

‘Long term potentiation’

A

The strengthening of synapses due to repetitive behaviours

228
Q

Receptors involved in long term potentiation

A

NMDA glutamate receptors

229
Q

Define consciousness

A

Ability to react appropriately to stimuli in the outside world

230
Q

What does an EEG measure?

A

Voltages across the cerebral cortex

231
Q

EEG appearance when awake and alert

A

Low amplitude and high frequency

232
Q

EEG appearance when drowsy and close to sleep

A

High amplitude and low frequency

233
Q

Two functions of sleep

A

Growth - release of growth hormone

Wound repair - effect on the immune system

234
Q

Three effects of lack of sleep

A

Lack of concentration
Hypertension - risk of CVD
Obesity - reduced release of leptin and reduced sensation of satiety

235
Q

How often do the stages of the sleep cycle repeat?

A

Stages 1-4 repeat every 90 minutes

236
Q

Noradrenaline, serotonin and Ach levels when asleep vs. awake

A

These are high when awake and low when asleep

237
Q

Function of REM sleep

A

Consolidation of memories

Removal of junk

238
Q

Drugs to treat insomnia

A

Benzodizepines and Z drugs

239
Q

Effect of dopamine on sleep

A

High levels of dopamine prevents sleep

240
Q

Classical condition vs. operant conditioning

A

Classical - pairing of two stimuli to illicit a conditioned response
Operant - learning is controlled by consequences (negative and positive reinforcers)

241
Q

Four components of classical conditioning

A

Unconditioned stimulus - food
Conditioned stimulus - bell
Unconditioned response - salivating in response to food
Conditioned response - salivating in response to bell

242
Q

Define Garcia effect

A

Avoiding eating certain foods/drink due to a previous unpleasant experience

243
Q

Define theory of tolerance

A

Ceasing of the conditioned stimulus does not stop the association between conditioned stimulus and response

244
Q

Define social learning

A

Watching what other people do and how they are rewarded for this and copying their behaviour

245
Q

What are the two most common waves seen in an ECG and when specifically are they seen?

A

Alpha - seen in most awake adults

Beta - seen in awake and alert (mental task) adults

246
Q

What causes a change in alpha waves in an awake patient?

A

Alpha waves are neutral when eyes are closed
Opening of the eyes causes a change in the frequency and the amplitude decreases
Mental activity causes the amplitude of the alpha waves to increase

247
Q

Alpha and beta waves when eyes are open vs. when eyes are shut

A

Eyes are closed - amplitude of the alpha waves is high and amplitude of beta waves is low
Eyes are open - amplitude of alpha waves is low and amplitude of beta waves is high

248
Q

How is pain tolerance ratio calculated?

A

Experimental time (may be mean)/control time (may be mean)

Year 2 BB (36 decks)

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